BrightFocus-funded Research May Contribute to New Treatments for Hereditary Glaucoma
Inhibiting the protein Grp94 could lead to new treatment for the sight-robbing eye disease
October 10, 2012
Source: The Journal of Biological Chemistry
Dr. Chad Dickey of the USF Health Byrd Alzheimer's Institute was principal investigator for this study concerning new treatments for hereditary glaucoma.
The photo is provided courtesy of USF Health Byrd Alzheimer's Institute
A discovery, published in The Journal of Biological Chemistry, could result in new treatments for some hereditary cases of glaucoma, an eye disease that is a primary cause of blindness, said principal investigator Chad Dickey, Ph.D., associate professor of molecular medicine at the USF Health Byrd Alzheimer's Institute.
“When mutated, the glaucoma-causing protein [myocilin] becomes toxic to a cell network known as the trabecular meshwork cells that regulate pressure within the eye,” Dickey said. “Once these cells die, the ocular pressure increases, causing glaucoma.”
Genetic defects of myocilin account for approximately 8 to 36 percent of hereditary juvenile-onset glaucoma and 5 to 10 percent of adult-onset hereditary glaucoma.
The researchers suggest that mutant myocilin interacts with the "chaperone" protein called Grp94, which makes the mutant protein highly resistant to degradation and clearance by the cell's normal quality control protection system. Ultimately, this buildup of mutant myocilin leads to the death of eye cells important for vision. By adding a Grp94 inhibitor to cultured cells, Dr. Dickey's team found that the mutant myocilin was once again cleared from the cells. So, the future development of targeted therapies to inhibit Grp94 may be beneficial for patients suffering from glaucoma due to problems with the myocilin protein.
Adapted from the University of South Florida
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